Although the effects of treatment of animals with tumor viruses and carcinogenic chemicals are well known, the mechanism of carcinogenesis is not well understood. Recent estimates have suggested that most human cancer originates from carcinogenic chemicals in the environment. This project is aimed at understanding the mechanism of action of such agents at the molecular level, using a previously well-characterized system in E. coli. A typical carcinogen, ultraviolet light, induces the expression of both viral and cellular genes in E. coli. E. coli lysogenic for phage lambda is induced to produce virus particles by a number of carcinogens. It is known that transcription of the lytic genes of phage lambda is turned off in lysogenic cells by the phage repressor that binds to the viral DNA but is destroyed by a cell mechanism in induction. Recent evidence suggests a cell protease may cleave repressor. It is our intention to obtain experimental proof for this mechanism. A similar cleavage of cell proteins could lead to identical induction of an error-prone DNA repair process that accounts for the mutagenic effects of carcinogens. Possible induction mechanisms other than proteolytic cleavage of proteins will also be investigated, the proteins that control these processes will be identified as well as the DNA lesion that signals induction to occur. It is hoped that these studies uncover basic mechanisms in control of cellular functions that can account for the action of viruses and carcinogens on animal cells.